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EVOLUTION OF LATE‐LIFE MORTALITY IN DROSOPHILA MELANOGASTER
Author(s) -
Rose Michael R.,
Drapeau Mark D.,
Yazdi Puya G.,
Shah Kandarp H.,
Moise Diana B.,
Thakar Rena R.,
Rauser Casandra L.,
Mueller Laurence D.
Publication year - 2002
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/j.0014-3820.2002.tb00124.x
Subject(s) - biology , mutation accumulation , pleiotropy , drosophila melanogaster , natural selection , evolutionary biology , reproduction , mutation rate , longevity , population , mortality rate , genetics , demography , gene , phenotype , sociology
.— Aging appears to cease at late ages, when mortality rates roughly plateau in large‐scale demographic studies. This anomalous plateau in late‐life mortality has been explained theoretically in two ways: (1) as a strictly demographic result of heterogeneity in life‐long robustness between individuals within cohorts, and (2) as an evolutionary result of the plateau in the force of natural selection after the end of reproduction. Here we test the latter theory using cohorts of Drosophila melanogaster cultured with different ages of reproduction for many generations. We show in two independent comparisons that populations that evolve with early truncation of reproduction exhibit earlier onset of mortality‐rate plateaus, in conformity with evolutionary theory. In addition, we test two population genetic mechanisms that may be involved in the evolution of late‐life mortality: mutation accumulation and antagonistic pleiotropy. We test mutation accumulation by crossing genetically divergent, yet demographically identical, populations, testing for hybrid vigor between the hybrid and nonhybrid parental populations. We found no difference between the hybrid and nonhybrid populations in late‐life mortality rates, a result that does not support mutation accumulation as a genetic mechanism for late‐life mortality, assuming mutations act recessively. Finally, we test antagonistic pleiotropy by returning replicate populations to a much earlier age of last reproduction for a short evolutionary time, testing for a rapid indirect response of late‐life mortality rates. The positive results from this test support antagonistic pleiotropy as a genetic mechanism for the evolution of late‐life mortality. Together these experiments comprise the first corroborations of the evolutionary theory of late‐life mortality.